How a Heart Fails

July 12, 2015 by

July 10, 2015

By Medical Discovery News

A heart

What exactly causes a heart to fail? It may come down to a simple protein, which scientists recently identified as having an important role in how a heart goes from weakening to failing.

Your heart is a strong, muscular pump slightly larger than your fist that pushes blood through your body. Blood delivers the necessary oxygen and nutrients to all cells in all the organs. Every minute, your heart pumps five quarts of blood. Human hearts have four chambers: two atria on top and two ventricles on bottom. Oxygenated blood leaves the lungs, enters the left atrium, moves to the left ventricle, and is then pumped out of the heart to the rest of the body. After it circulates, blood returns to the heart, enters the right atrium, moves to the right ventricle, and is then sent back to the lungs for a fresh dose of oxygen. Although your heart beats 100,000 times each day, the four chambers must go through a series of highly organized contractions to accomplish this.

Any disruption of this process can have serious consequences such as heart failure, which is clinically defined as a chronic, progressive weakening of the heart’s ability to circulate enough blood to meet the body’s demands. To compensate, the heart enlarges, which increases contractions and the volume of blood pumped. Blood vessels elsewhere in the body narrow to keep blood pressure normal. Blood can even be diverted from less important organs, ensuring more vital organs like the brain and heart are satisfied. However, such responses mask the underlying problem: the weakening heart, which continues to worsen. Ultimately, the body can no longer compensate for the heart, which is when it will start to fail.

Scientists at the University of California, San Diego School of Medicine studied the cellular changes in weakened hearts to better understand the transition from the compensatory stage, when it works harder to pump blood, to the decompensation, when it fails to pump blood sufficiently. They were especially interested in a RNA-processing protein called RBFox2 because it is involved in the heart’s early development and its continuing functions. When genes are expressed, DNA is transcribed into RNA, which is then processed and eventually used to make proteins such as RBFox2.

Sure enough, levels of RBFox2 were dramatically reduced in the hearts of mice with a condition similar to heart failure. Then they genetically engineered mice without RBFox2, which developed symptoms of heart failure. Not only are low levels of this protein connected to weakened heart muscle, without enough of it, the body cannot compensate and the heart declines more quickly. However, we still don’t know why levels of RBFox2 decline during the transition to the decompensatory phase of heart failure.

In the future, this research might be used to develop treatments that reverse the decline of RBFox2 and effectively slow or prevent heart failure.

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Where’s the Beat?

January 13, 2015 by

Jan. 9, 2015

By Medical Discovery News

Where's the Beat

Have you ever noticed when someone in the audience can’t clap along with a beat at a concert? Well, it turns out that beat deafness actually exists. The first case was documented nearly five years ago, identified in a 26-year-old man who could not follow the beat at all when listening to music. Chances are, you don’t have it, though. Beat deafness is a form of musical brain disorder that is extremely rare.

Sometimes, audience members get so off beat that performers stop in an effort to get back on track. That in part inspired a group of neuroscientists in Montreal to look for people who felt they had no sense of the beat. After screening dozens of people, only one, Mathieu, was found to have true beat deafness.

Mathieu loves music, studies guitar, and once had a job as an amusement park mascot that involved dancing, which by his own admission did not go so well. “I just can’t figure out what’s rhythm, in fact,” Mathieu said. “I just can’t hear it, or I just can’t feel it.” However, he can follow the beat if he watches someone else. He could also follow the beat of a metronome, indicating that he did not have a movement disorder. In one test, Mathieu was asked to bounce or bend his knees to the beat of different kinds of music while holding a Wii controller that logged his movements. His results were compared to normal people who could identify the beat. After being tested with merengue, pop, rock, belly dancing, and techno music, he was only able to follow the distinct and obvious beats of techno music.

Rhythm appears to be sensed by a widespread network in the brain, not in a defined region like speech. Rhythm itself consists of several temporal elements such as pattern, meter, and tempo. Meter is the repeating cycles of strong and weak beats, pattern is the intervals at each point in time, and tempo is the frequency of underlying pulses. Each of these appears to be sensed differently and has been mapped to neural systems within the brain through positron emission tomography (PET) scans. It also appears that only humans can process meter, whereas other species may be able to process pattern and perhaps tempo. Distinct and distributed neural systems are also involved in sensing and processing other elements of music such as melody, harmony, and timbre.

When it comes to dancing to music, though, neural processing of rhythm is only the beginning. Orchestrated or planned movements start in the motor cortex, which is divided into sections that each govern a different part of the body. Signals from the motor cortex travel down 20 million nerve fibers in the spinal cord to an arm or finger, telling it to respond in a particular way.

To achieve a rhythmic, well-coordinated style of dance, the brain must coordinate all these efforts for joints to act in proper order and muscles to contract to the perfect degree. So as complex as all this is, perhaps it is not all that surprising that some people are better dancers than others.

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I Spy for Heart Disease

August 29, 2014 by

Aug. 29, 2014

By Medical Discovery News

Heart in chest

While a shrink ray like the kind used in science fiction is still stuck in the future, miniature devices are not. Tiny devices have been created to perform a variety of tasks, from an implantable telescope to improve vision in those with macular degeneration to the new pacemaker in clinical trials that is about the size of a large vitamin pill. Now, researchers have developed a catheter-based device smaller than the head of a pin that can provide real-time 3D images of the heart, coronary arteries, and other blood vessels. This is an important invention as the casualties of heart disease continue to rise. Statistically, one in four people will have a heart attack. 

Many Americans are at risk for developing coronary artery disease (CAD) due to the buildup of cholesterol and plaque. If there is a rupture or breakage of the plaque, creating a blood clot, that can result in a heart attack with little to no warning. Traditional diagnostic tests such as stress tests and echocardiograms show how much blood is flowing to the heart. If there are regions of the heart that are not getting as much blood as others, it might be a sign of clogged coronary arteries. However, blood flow can also appear to be normal even with plaque buildup.

Currently, there are a variety of methods that provide images of what is going on inside arteries, including magnetic resonance imaging (MRI), multi-detector Computerized Tomography (CT) scans, and injecting an iodine-based contrast agent into arteries through a catheter. But all these look at the inside of the body from the outside, which is why this new device gives an unprecedented way of viewing the heart.

This invention combines ultrasound imaging with computer processors on a single chip only 1.4 millimeters wide. The body’s signals are processed on the chip then transmitted through 13 tiny cables to a computer monitor, so doctors have a visual of the heart and arteries. The prototype took 60 images per second using very little power, therefore generating little heat. This would allow cardiologists to take real-time images of blood vessels in and around the heart to more precisely determine the extent of blockages. These images also have much higher resolution compared to those taken with machines outside the body.

The next step is to conduct studies using the device on animals to determine its safety and efficacy and to develop potential applications of this technology. Eventually, this data will be submitted to the Food and Drug Administration (FDA) to gain permission to perform clinical trials on humans. Extensive testing will be required before the FDA will approve the device for general use. The developers, a group of engineers at the Georgia Institute of Technology, are also working to shrink the device even further to .4 millimeters so it can generate images of even smaller blood vessels.

Having clearer images of blood vessels would allow surgeons to have a more complete understanding of the blockage they are dealing with before they operate. Hopefully, in the future use of this device will prevent heart attacks and save many people’s lives.

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Heart Heal Thyself

March 11, 2012 by

By Medical Discovery News

Nov. 26, 2011

Heart Heal Thyself

The vast majority of human cells regenerate: skin, stomach lining, red blood cells, bone cells, liver cells and the list goes on. But certain cells either do not regenerate at all, or take years to do so. Among these cells is a heart muscle cell called cardiomyocyte.

Starting at birth, these cells regenerate at just one percent a year, and by the time of death only half of the original heart muscle cells are replaced. That’s why damage from a heart attack is considered permanent. Within minutes, depending on where the blockage occurred, cardiomyocytes are either damaged or dead from a lack of oxygen-rich blood. The heart begins to produce replacement cells, but not fast enough. So, instead of new muscle cells, scar tissue forms, compromising the heart’s ability to pump blood. The amount of lost pumping ability depends on the size and location of the scar.

Scientists have spent years looking for a way to stop, slow or heal this damage, and they’re making headway. Researchers at the University of Texas Southwestern Medical Center in Dallas are focused on a small protein called Thymosin beta-4, or TB4. When the heart develops inside a human embryo, TB4 is made. This protein encourages the growth of cardiomyocytes, and stimulates the growth of blood vessels. Could this protein be used somehow to heal a damaged heart? Research with mice show this may be a promising new therapy.

Scientists have known the outer layer of the heart holds heart progenitor stem cells from which new cardiac cells are produced. They’re called epicardium-derived progenitor cells or EDPCs . These cells are usually dormant, but the UT researchers found when they injected the mice with TB4 it gave EDPCs a jump start. Within 24 hours, TB4 not only began to reduce the number of cardiomyocytes killed during a heart attack, but it also stimulated dormant progenitor cells to regenerate those that did die, reducing scar formation.

Over the long term, the mice also showed new blood vessel formation in the heart, bypassing blocked vessels. The hope is TB4 will prove to be just as effective in larger mammals and eventually, humans. Ideally, high risk patients would be treated prior to developing a heart attack as a preventative to prime the heart for repair, and possibly to treat the heart after an attack as well.

TB4 is already in clinical trials, and studies are also in progress to find molecules with the same but even more potent and specific effects.  The goal among researchers is to provide TB4 or a drug with similar effects to the public in 10 years. In America alone, one million people suffer heart attacks every year and that number is only expected to grow.

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